CD27 mediates interleukin-2-independent clonal expansion of the CD8+ T cell without effector differentiation.
The clonal expansion of antigen-specific CD8(+) T cells in response to microbial infections is essential for adaptive immunity. Although IL-2 has been considered to be primarily responsible for this process, quantitatively normal expansion occurs in the absence of IL-2 receptor signaling. Here, we show that ligating CD27 on CD8(+) T cells that have been stimulated through the T cell receptor causes their expansion in the absence of IL-2 by mediating two distinct cellular processes: enhancing cell cycling and promoting cell survival by maintaining the expression of IL-7 receptor alpha. This pathway for clonal expansion of the CD8(+) T cell is not associated with the development of a capacity either for production of IFN-gamma or for cytotoxic T lymphocyte function and, therefore, is uncoupled from differentiation. Furthermore, ligating CD27 increases the threshold concentration at which IL-2 induces IFN-gamma-producing capability by the CD8(+) T cell, suggesting that CD27 signaling may suppress effector differentiation. Finally, CD8(+) T cells that have been stimulated by the TCR/CD27 pathway maintain their capacity for subsequent expansion and effector differentiation in response to a viral challenge in vivo. Thus, the TCR/CD27 pathway enables the CD8(+) T cell to replicate by a process of self-renewal, which may contribute to the continuous generation of new effector CD8(+) T cells in persistent viral infections.[1]References
- CD27 mediates interleukin-2-independent clonal expansion of the CD8+ T cell without effector differentiation. Carr, J.M., Carrasco, M.J., Thaventhiran, J.E., Bambrough, P.J., Kraman, M., Edwards, A.D., Al-Shamkhani, A., Fearon, D.T. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
